Lupus nephritis occurs in a sub-population of patient with systemic lupus erythematosus (SLE) and is one of the most severe complications of SLE, associated with significant morbidity and mortality. Systemic lupus erythematosus (SLE) is an autoimmune disorder involving multiple organs injury due to autoantibody production and abnormal cell immunity. The cumulative risks of end stage renal failure were particularly high in patients with severe lupus nephritis, the histopathology of which comprises distinct patterns of injury that were initially defined by the World Health Organization Classification of 1982 as category III, category IV, and categories Vc and Vd. The exact mechanisms for the development or the progression of lupus nephritis remain unclear. There is no definitive treatment for lupus nephritis. Current therapies for lupus nephritis are various combinations of corticosteroids with other cytotoxic agents or immunomodulators, but many of these have various side effects.
Ginsenosides, the main active ingredients of ginseng, are known to have a variety of pharmacological activities, e.g. antitumor, antidiabetic, antifatique, antiallergic and antioxidant activities. Ginsenosides share a basic structure, composed of gonane steroid nucleus having 17 carbon atoms arranged in four rings. Ginsenosides are metalized in the body, and a number of recent studies suggest that ginsenoside metabolites, rather than naturally occurring ginsenosides, are readily absorbed in the body and act as the active components. Among them, ginsenoside M1 is known as one metabolite of protopanaxadiol-type ginsenosides via the gypenoside pathway by human gut bacteria. Until now, no prior art references report the effect of ginsenoside M1 in treatment of lupus nephritis.